A novel regulatory mechanism of naringenin through inhibition of T lymphocyte function in contact hypersensitivity suppression
A novel regulatory mechanism of naringenin through inhibition of T lymphocyte function in contact hypersensitivity suppression
复制标题
柚皮素通过抑制 T 淋巴细胞功能来抑制接触性超敏反应的新型调节机制。
DOI:
10.1016/j.bbrc.2010.05.065
复制
发表时间:
2010-06-25
影响因子:
3.1
通讯作者:
Xu, Qiang
中科院分区:
文献类型:
--
作者:
Fang, Feng;Tang, Yijun;Xu, Qiang
Naringenin, a flavonoid in grapefruits and citrus fruits, has been reported to exhibit anti-inflammatory and anti-oxidative activities. Contact hypersensitivity (CHS) is a T cell-mediated immune reaction, and the factors released from macrophages also contribute to this response. Previous studies showed that naringenin suppressed CHS by inhibiting activation and migration of macrophages. However, little is known about naringenin's effects on T lymphocytes. Our study indicated that naringenin potently suppressed picryl chloride (PCI)-induced contact hypersensitivity by inhibiting the proliferation and activation of T lymphocytes. in vitro, both of the activated hapten-specific T cells and the T cells stimulated with anti-CD3/anti-CD28 showed growth arrest after naringenin treatment. Furthermore, naringenin reduced CD69 (the protein level) and cytokines such as IL-2, TNF-alpha, and IFN-gamma (the mRNA level) expressions which highly expressed by activated T cells. Meanwhile, naringenin also induced T cell apoptosis by upregulation of Bax, Bad, PARP, cleaved-caspase 3 and downregulation of phosphorylated Akt, Bcl-2. These findings suggest that, besides its anti-inflammatory activities in macrophages, naringenin also showed inhibitory effects on the activation and proliferation of T cells to alleviate symptoms of contact hypersensitivity. (C) 2010 Elsevier Inc. All rights reserved.